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A Magnetic Resonance Imaging-based Computational Protocol for Analysis of Plaque Morphology and Hemodynamics in Patients with Carotid Artery Stenosis
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Pathophysiology and risk factors of cervical artery dissection: what have we learnt from large hospital-based

Stéphanie Debette1

  • 1aDepartment of Neurology, Lariboisière Hospital bInserm Unit U740 cParis 7 University, DHU Neurovasc Sorbonne Paris-Cité, Paris, France dDepartment of Neurology, Framingham Heart Study, Boston University School of Medicine, Boston, Massachusetts, USA.

Current Opinion in Neurology
|December 5, 2013
PubMed

Insights

Cervical artery dissection (CeAD) is a leading cause of stroke in younger adults. Research identifies hypertension and migraine as key risk factors, while genetic causes remain unclear.

Area of Science:

  • Neurology
  • Vascular Medicine
  • Genetics

Background:

  • Cervical artery dissection (CeAD) is a significant cause of ischemic stroke in young and middle-aged individuals.
  • Recent research has enhanced understanding of CeAD mechanisms and risk factors.

Purpose of the Study:

  • To review current knowledge on the pathophysiology and risk factors of CeAD.
  • To highlight gaps in understanding, particularly regarding genetic influences.

Main Methods:

  • Analysis of large collaborative projects and multicenter series of CeAD patients.
  • Comparison of CeAD patients with healthy controls and stroke patients of other causes.
  • Review of associations with fibromuscular dysplasia and reversible cerebral vasoconstriction syndrome.

Main Results:

  • Arterial wall weakness at the media-adventitia border is implicated in CeAD.
  • Confirmed risk factors include hypertension, migraine (especially without aura), cervical trauma, and recent infection.
  • Hypercholesterolemia and overweight status show inverse associations with CeAD.
  • Potential differences in pathophysiology between carotid and vertebral dissection are suggested.
  • Associations with fibromuscular dysplasia and reversible cerebral vasoconstriction syndrome are noted.

Conclusions:

  • Large patient cohorts have improved understanding of CeAD pathophysiology and risk factors.
  • Molecular and genetic mechanisms underlying CeAD require further investigation.
  • Ongoing genetic studies are expected to provide new insights into the biological basis of CeAD.
Abstract

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